A Decade of Changing Perceptions about Neuropeptides

Kastin, Abba J.; Banks, William A.; Zadina, James E.

doi:10.1111/j.1749-6632.1990.tb48348.x

Cited by 30 publications

(8 citation statements)

References 54 publications

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“…In agreement with previous reports (6), oxytocin, microinjected into the NTS, produced significant vasopressor and tachycardic response that showed a dose–response relationship with regard to the tachycardic response. The inverted U‐shaped dose–response curves observed for the mean arterial blood pressure responses is a common phenomenon seen in responses to peptides (20, 21, 33). The mechanism of action of oxytocin in the NTS is probably an activation of the sympathetic output more than an inhibition of the parasympathetic output since microinjections of oxytocin in the DMV cause bradycardia, an effect blocked by an oxytocin antagonist and by atropine (5).…”

Section: Methodsmentioning

confidence: 98%

Antagonistic Oxytocin/α₂‐Adrenoreceptor Interactions in the Nucleus Tractus Solitarii: Relevance for Central Cardiovascular Control

́az‐Cabiale

Narváez

Garrido

et al. 2000

J Neuroendocrinology

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The modulation of the central cardiovascular effects of alpha2-adrenoceptor activation by oxytocin in the nucleus tractus solitarii has been evaluated by cardiovascular analysis and by quantitative receptor autoradiography. Microinjections in the nucleus tractus solitarii of a threshold dose of oxytocin effectively and significantly counteracted the vasodepressor and bradycardic actions of an ED50 dose of the alpha2-adrenoceptor agonist clonidine. The coinjection of a threshold dose of oxytocin with a threshold dose of clonidine did not produce any changes in the mean arterial pressure but a tachycardic response was observed. Receptor autoradiographical experiments showed that oxytocin (3 nM) significantly increased the Kd and Bmax values of [3H]p-aminoclonidine binding sites in the nucleus tractus solitarii compatible with a possible antagonistic interaction with the alpha2-adrenoceptors, and this effect was blocked by the presence of the specific oxytocin receptor antagonist 1-deamino-2-D-Tyr-(OEt)-4-Thr-8-Orn-oxytocin. These findings suggest the existence of an antagonistic oxytocin/alpha2-adrenoceptor interaction in nucleus tractus solitarii that may be of relevance for the demonstrated modulation of alpha2-adrenoceptor induced cardiovascular responses by oxytocin.

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Section: Methodsmentioning

confidence: 98%

Antagonistic Oxytocin/α₂‐Adrenoreceptor Interactions in the Nucleus Tractus Solitarii: Relevance for Central Cardiovascular Control

́az‐Cabiale

Narváez

Garrido

et al. 2000

J Neuroendocrinology

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“…Therefore, PYY would have to negotiate the BBB to reach the receptors in the arcuate nucleus. The BBB controls the exchange of peptides and regulatory proteins between the central nervous system (CNS) and blood (Banks and Kastin, 1985, 1996Kastin et al, 1990;Begley, 1992;Brownlees and Williams, 1993) and has emerged as a major regulator of communication between the central nervous system and the peripheral tissues . One area where this regulation is particularly clear is in the area of feeding hormones.…”

mentioning

confidence: 99%

Characterization of Blood-Brain Barrier Permeability to PYY_3-36 in the Mouse

Nonaka

Shioda²,

Niehoff³

et al. 2003

J Pharmacol Exp Ther

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164

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Peptide YY 3-36 (PYY) has emerged as an important signal in the gut-brain axis, with peripherally administered PYY affecting feeding and brain function. For these effects to be direct, PYY would have to cross the blood-brain barrier (BBB). Here, we determined the permeability of the BBB to PYY radioactively labeled with 131 I (I-PYY). Multiple-time regression analysis showed the unidirectional influx rate (K i ) from blood-to-brain for I-PYY to be 0.49 Ϯ 0.19 l/g-min, a rate similar to that previously measured for leptin. Influx was not inhibited by 1 g/ mouse of unlabeled PYY, suggesting PYY crosses the BBB by transmembrane diffusion. About 0.176% of the i.v.-injected dose of I-PYY was taken up by brain, an amount similar to that for other peptides important in gut-brain communication. Capillary depletion showed that 69% of I-PYY crossed the BBB to enter the parenchymal space of the brain, and high-performance liquid chromatography demonstrated that the radioactivity in this space represented intact I-PYY. After intracerebroventricular injection, I-PYY crossed from brain to blood by the mechanism of bulk flow. We conclude that PYY crosses in both the blood-to-brain and brain-to-blood directions by nonsaturable mechanisms. Passage across the BBB provides a mechanism by which blood-borne PYY can affect appetite and brain function.Peptide YY has emerged as a major component of the gut-brain axis regulation of feeding, body weight, and nutritional status. It is a member of the neuropeptide Y family that includes neuropeptide Y (NPY), pancreatic polypeptide, and two forms of peptide YY, a 36-amino acid form and the 3-to 36-amino acid form (PYY). Each of these forms acts through the NPY receptors (Larhammar, 1996). For example, PYY is an agonist at the Y1/Y2 receptors and promotes feeding, whereas PYY 3-36 is an antagonist at the Y2 receptor and inhibits feeding (Grandt et al., 1994b). PYY is abundant in human blood (Grandt et al., 1994a) and is released from endocrine cells found throughout the small intestine in proportion to the caloric content of a meal (Ekblad and Sundler, 2002). Blood-borne PYY can affect appetite and influence neuronal activity at the arcuate nucleus (Batterham et al., 2002).The arcuate nucleus in the adult is clearly separated from the peripheral circulation and median eminence by the endothelial and ependymal arms of the blood-brain barrier (BBB) (Rethelyi, 1984;Peruzzo et al., 2000). Therefore, PYY would have to negotiate the BBB to reach the receptors in the arcuate nucleus. The BBB controls the exchange of peptides and regulatory proteins between the central nervous system (CNS) and blood (Banks and Kastin, 1985, 1996Kastin et al., 1990;Begley, 1992;Brownlees and Williams, 1993) and has emerged as a major regulator of communication between the central nervous system and the peripheral tissues . One area where this regulation is particularly clear is in the area of feeding hormones. Leptin (Banks et al., 1996), ghrelin (Banks et al., 2002c), melanocyte-stimulating hormone (Wilson ...

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“…We should also note that all the mentioned activities are probably of a strictly peripheral origin, because substances like histamine, acetylcholine and kinins do not pass the blood-brain barrier (Ishay et al 1974b). In contrast, mastoparan, and similar polypeptides probably does pass the blood-brain barrier, so that its effect is central as well as peripheral (Kastin et al 1979(Kastin et al & 1990Strand et al 1990).…”

Section: Discussionmentioning

confidence: 98%

Cardiovascular Haemodynamics of Oriental Hornet Venom Sac Extract

Rubin

Duvdevani

Ishay

1993

Pharmacology & Toxicology

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The effects of hornet venom sac extract on the functioning of the cardiovascular system was assessed in dogs by concomitant examination of the following parameters: Systemic blood pressure, blood pressure and the dp/dt derivative of the left ventricle of the heart, heart rate, direct measurement of the left ventricular wall thickness, cardiac output, and body temperature. The effect of adult hornet venom sac extract on the canine cardiovascular system was rapid and led to a sharp drop in the systemic blood pressure, a similar drop in the pressure and dp/dt derivative in the left ventricle, to bradycardia, immediate thickening of the left ventricular wall and to an immediate rise in the cardiac output. As for the canine temperature, this dropped immediately following the administration of venom sac extract and remained at the new low level for at least 30 min. The smaller molecular weight components (less than 10 kilodalton) in venom sac extract have been found to be responsible for the immediate effects of venom sac extract on the cardiovascular system. On the other hand the high‐molecular weight components exert more delayed effects which lead to a cumulative disturbance of cardiac function.

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A Decade of Changing Perceptions about Neuropeptides

Cited by 30 publications

References 54 publications

Antagonistic Oxytocin/α₂‐Adrenoreceptor Interactions in the Nucleus Tractus Solitarii: Relevance for Central Cardiovascular Control

Antagonistic Oxytocin/α₂‐Adrenoreceptor Interactions in the Nucleus Tractus Solitarii: Relevance for Central Cardiovascular Control

Characterization of Blood-Brain Barrier Permeability to PYY_3-36 in the Mouse

Cardiovascular Haemodynamics of Oriental Hornet Venom Sac Extract

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A Decade of Changing Perceptions about Neuropeptides

Cited by 30 publications

References 54 publications

Antagonistic Oxytocin/α2‐Adrenoreceptor Interactions in the Nucleus Tractus Solitarii: Relevance for Central Cardiovascular Control

Antagonistic Oxytocin/α2‐Adrenoreceptor Interactions in the Nucleus Tractus Solitarii: Relevance for Central Cardiovascular Control

Characterization of Blood-Brain Barrier Permeability to PYY3-36 in the Mouse

Cardiovascular Haemodynamics of Oriental Hornet Venom Sac Extract

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Product

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Antagonistic Oxytocin/α₂‐Adrenoreceptor Interactions in the Nucleus Tractus Solitarii: Relevance for Central Cardiovascular Control

Antagonistic Oxytocin/α₂‐Adrenoreceptor Interactions in the Nucleus Tractus Solitarii: Relevance for Central Cardiovascular Control

Characterization of Blood-Brain Barrier Permeability to PYY_3-36 in the Mouse